Renal prostacycline (PGI2) and oxidative stress are known to be important factors that effect the natriurezis and diuresis. 8-iso prostaglandin F2α± (8-isoprostane), a member of F2-isoprostanes, is ...formed from the nonenzymatic reaction of arachidonic acid and oxygen radicals in vivo and in vitro, and also it is a marker of oxidative stress in vivo. The aim of this study is to determine the role of renal PGI2 and 8-isoprostane in a salt and nitric oxide (NO) inhibition-induced hypertension model. Rats were distributed equally among four groups (n = 6 per group). Control rats were given normal salt diet (0.32%); high-salt (HS) rats were given high salt diet (3.2%); NG-nitro-L-arginine (L-NNA) rats were given normal salt diet and 25 mg kg L-NNA; HS+L-NNA rats were given high salt diet and 25 mg kg L-NNA. Rats were placed in individual metabolic cages for 17 days. Systolic blood pressure (SBP) was measured at days initial, 7th and 14th .Urinary 8-isoprostane and PGI2 levels were analyzed. Salt- loading alone did not change SBP values. The average SBP in L-NNA and HS+L-NNA groups were shown to significantly enhance compared to initial and day 7th in the same groups, respectively. The levels of 8-isoprostane in the HS+L-NNA group was significantly enhanced compared to the other groups. L-NNA or HS diet alone did not change the levels of 8-isoprostane compared to the control group. L-NNA alone did not change PGI2 levels in urine compared to the control. PGI2 levels in the HS, and the HS+L-NNA group was significantly higher compared to the control group. This study concluded that NOS inhibition plus salt-loading induced oxidative stress and increased renal PGI2. Also, it is suggested that augmented oxidative stress may aggravate the hypertension. But the renal synthesis of PGI2 is increased in order to augment the diuresis and natriuresis without the effect of blood pressure (BP).
Objective:
The purpose of the present study was to evaluate the effects of melatonin on biochemical and cardiovascular changes resulting from exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), a ...polychlorinated dibenzo-para-dioxin.
Methods:
A total of 24 Sprague-Dawley rats were divided equally into the following four groups: (1) control group was administered with 0.5 mL corn oil by gavage and 0.5 cc vehicle of melatonin (proportionally nine parts physiological serum + one part ethyl alcohol) intraperitoneally for 4 weeks, (2) the melatonin group was given 5 mg/kg/day melatonin intraperitoneally for 4 weeks, (3) the TCDD group was given 500 ng/kg/day TCDD by gavage for 4 weeks and (4) the TCDD + melatonin group was given TCDD (500 ng/kg/day) by gavage and melatonin (5 mg/kg/day) intraperitoneally simultaneously for 4 weeks. Systolic blood pressure was evaluated by the tail-cuff method. Vascular responses to phenylephrine and acetylcholine were evaluated in the isolated thoracic aortas.
Results:
TCDD not only augmented the systolic blood pressure but also increased the contractile responses to phenylephrine in aorta. Melatonin reversed the blood pressure augmented by TCDD and decreased the contractile responses to phenylephrine in aorta. TCDD induced an increase in the malondialdehyde levels in kidney tissue and melatonin did not change it. Therefore, TCDD caused a decrease in glutathione levels in kidney tissues and melatonin reversed it.
Conclusion:
Present data demonstrated that TCDD may lead to an increase in blood pressure via increased renal oxidative stress and vascular reactivity. However, melatonin might ameliorate the blood pressure disturbed by TCDD in part by decreasing the oxidant activity induced by TCDD.
Summary Aim Liver fibrosis is a reversible wound-healing response that occurs following liver injury. In this study, we aimed to investigate the possible protective effects of L -carnitine, N ...-acetylcysteine and genistein in liver fibrosis induced by carbon tetrachloride (CCl4 ). In addition, the effects of these agents were compared in the same study. Methods In this study, rats were randomly allocated into 8 groups, consisting of 10 rats each, as follows: a control group, CCl4 , L -carnitine, N -acetylcysteine, genistein, CCl4 and L -carnitine, CCl4 and N -acetylcysteine, and CCl4 and genistein. At the end of 6 weeks, blood and liver tissue specimens were collected. Alanine aminotransferase (ALT); aspartate aminotransferase (AST); complete blood count, tumor necrosis factor-α (TNF-α); platelet-derived growth factor-BB (PDGF-BB); interleukin-6 (IL-6); liver glutathione level; oxidant/antioxidant status; scores of hepatic steatosis, necrosis, inflammation, and fibrosis; and the expression of α-smooth muscle actin were studied. Results Although the ALT and AST values in the group administered CCl4 were significantly higher than in all the other groups ( P < 0.05), there was no significant difference between the control group and the groups administered CCl4 combined with L -carnitine, N -acetylcysteine and genistein ( P > 0.05). There were significant differences in the levels of TNF-α, PDGF-BB and IL-6 ( P < 0.05) between the CCl4 group and the groups with L -carnitine, N -acetylcysteine and genistein added to CCl4. N -acetylcysteine and genistein had positive effects on the oxidant/antioxidant status and on liver necrosis and fibrosis scores. Conclusions In our study, L -carnitine, N -acetylcysteine and genistein showed significant protective effects in liver fibrosis induced by CCl4.
Convulsive status epilepticus (CSE) is very rarely observed after ischaemic stroke. Sodium valproate (SV) is one of the agents used in the treatment of CSE, but its role still controversial, and its ...degree of efficacy in treating CSE that develops following stroke is unclear.
We evaluated 19 patients who were treated with intravenous (IV) SV (20 mg/kg, 2 mg/kg/h-12h) after diazepam. Patients' modified Rankin scores (mRS), SE types, and changes in biochemical parameters after treatment were assessed.
CSE was successfully treated in 12 (63.15%) patients. Side effects such as hypotension and allergic reactions were observed in two patients. Refractory SE development was observed in 5 (29.4%) patients with high mRS (˃ 3). No significant deterioration in patients' laboratory evaluations, conducted before and after status, was observed.
SV may be safe and effective in the treatment of CSE observed after ischaemic stroke, especially in patients with low mRS.
This study is a placebo-controlled comparison of the response to alfuzosin treatment for lower urinary tract symptoms (LUTS) in patients with and without metabolic syndrome (MetS).
A total of 80 men ...with LUTS were included in the study. Patients had a maximum flow rate of <15 mL/sec, prostate volume of >20 mL, and International Prostate Symptom Score (IPSS) of >8. All eligible men (n=68) for evaluation were initially divided into two groups as MetS (n=34) and non-MetS (n=34) groups. Patients were further randomized to receive alfuzosin (10 mg/day) or placebo (n=17/group; a total of four groups). The outcome was measured at 12(th) week according to the changes from baseline in IPSS, quality of life (QoL) scores, maximum flow rate (Qmax), and postmictional residue.
Alfuzosin significantly improved LUTS in men with and without MetS compared with patients receiving placebo (p<0.05). Mean IPSS scores in treatment groups decreased significantly, whereas patients receiving placebo had no statistically significant difference (p>0.05). Similarly, alfuzosin treatment resulted in a significant increase in Qmax in patients with LUTS/benign prostatic enlargement when compared with patients in placebo group (p<0.05). Mean QoL scores measured by IPSS-QoL and QoL questionnaires also improved significantly in patients receiving alfuzosin for 3 months regardless of the presence of MetS (p<0.05).
Our results revealed that the presence of MetS in patients with LUTS did not impair the response to alfuzosin treatment.
The effects of AT2 receptor agonist novokinin on blood pressure, eNOS, NADPH oxidase, protein arginine methyltransferases (PRMTs), and Rho kinase in hypertension were investigated. Furthermore, in ...isolated thoracic aorta rings, contractile and dilator responses were studied.
To develop hypertension, L-NAME was administered intraperitoneally and salt was given with tap water (1%) for 4 weeks. Novokinin was administered intraperitoneally for the last 2 weeks. Blood pressures were measured using the tail-cuff method and enzyme levels by real-time polymerase chain reaction in aortic tissues.
Blood pressure increased significantly in hypertensive rats. Novokinin reduced the blood pressure in the hypertensive group. While the contractile responses to increasing doses of angiotensin II were increased, vascular reactivity (Emax) and sensitivity (EC50) to acetylcholine were decreased in hypertensive rats. In novokinin-treated hypertensive groups, the EC50 value decreased and the Emax value for acetylcholine significantly increased. The levels of Rho kinase and PRMT expression increased and the level of eNOS expression decreased in the hypertensive group. In novokinin-treated rats, ADMA, NADPH oxidase, and Rho kinase tended to decreased, but these changes did not reach statistical significance.
Although further studies are needed to determine its effectiveness, the AT2 agonist novokinin may be a novel agent that is promising in terms of protective effects for the treatment of hypertension.
The aim of this study is to investigate the effects of caffeic acid phenethyl ester (CAPE) on isoproterenol (ISO)-induced myocardial injury in hypertensive rats.
Rats were divided into 4 groups ...(n=29): Control group (n=8), L-NNA (NG-Nitro-L-arginine) group (n=8), L-NNA+ISO (L-NNA+isoproterenol) group (n=7) and L-NNA+ISO+CAPE (L-NNA+ISO + caffeic acid phenethyl ester) group (n=6). ISO (150 mg/kg/day) was given intraperitoneally (i.p.) once a day for 2 consecutive days (at the 12th and 13th days of L-NNA treatment). NG-Nitro-L-arginine (L-NNA) was given orally (25 mg/kg/day) in drinking water for 14 days. CAPE (10 μmol/kg/day) was given (i.p.) for 7 days after the first week. Systolic blood pressure (SBP) was evaluated by the tail-cuff method and biochemical analysis were performed using an autoanalyzer and a spectrophotometer.
SBP in all L-NNA-treated groups was found to be increased at seventh day. AST and LDH levels in LNNA+ISO group were significantly increased compared to control (AST: 125±5 vs. 105±2; LDH: 861±154 vs. 571±46 U/L respectively) (p<0.05). Also, ISO caused to extensive necrosis and mononuclear cell infiltration in hypertensive rat myocardium. CAPE application reversed the enhanced AST and LDH levels as well as the extensive necrosis and the mononuclear cell infiltration in LNNA+ISO+CAPE group compared LNNA+ISO.
According to our findings, it might be suggested that CAPE may be a favorable agent to protect the hypertensive myocardium from the injury induced by isoproterenol via mechanisms such as the induction of the antioxidant enzymes and the inhibition of lipid peroxidation.
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